Case Report - Obesity

CASE RECORD - 04

Name of the Hospital : National Hospital of Sri Lanka

Name of the consultant : Dr. Ruwan Ekanayaka
Consultant Cardiologist (MD, FRCP)


Case record : 04

Ward : 60-Unit 11

BHT No : 170119

Name of the patient : Mrs. I.J.P

Age : 59Years

Sex : Female

Address : 29/9B, Mulleriyawa North,
Angoda.

Date of admission : 01.02.2002.

Date of discharge : 07. 02. 2002.




HISTORY AND EXAMINATION
PRESENTING COMPLAINS
Swelling of the body,
Shortness of breath on exertion for two months duration.
Pin in the knee and difficulty in walking for four year.

HISTORY OF PRESENTING COMPLAINS
She suffered from swelling and pain in both knee joints for the last four years. This had an insidious onset and precipitated by pronged walking and standing. These symptoms were worse during the afternoon. Two month ago, she noted puffiness of her face and body. There was no noticeable degree of diurnal variation of the facial swelling and described it as a progressive and gradual phenomenon. Leg swelling was particularly more over the dorsum of left foot, which tend to increase during the afternoon and milder in the morning.

Shortness of breath, insidious in onset, gradually progressed over the time. Initially she could climb about 30-40 stirs without stopping, but now she was restricted to walk on flat ground for ten to twenty yards. She did not give a history of orthopnoea, paroxysmal nocturnal dyspnoea or associated palpitation. Exertion was not associated with chest tightness. In addition to the dyspnoea, her ability to walk significantly impaired by the associated knee joint pain and stiffness.

Her appetite seemed not change, but stated that she possibly taking more food than she was taking previously, especially for the last few months. There was no associated nausea or vomiting, and her bowel habit was unaltered with passing normal constituent stools at a frequency of once daily.

There was no history of cold intolerance or other symptoms suggestive of hypothyroidism. She did not give a history of easy bruising or poor wound healing. Her sleep was usually undisturbed and she waked with a fresh feeling (No evidence of sleep apnoea). There was no associated daytime sleepiness. She did not give a history of poly-uria or polydypsia.

She did not complain of significant and constant type of headache, especially during the hours of waking, when sneezing or coughing suggesting intracranial mass effect. There was no associated history of disturbed vision, for example blurring or double vision. There was no history of gallactorrhoea, loss of axillary or pubic hair or excess hair growth (hirsutism).

Knee joint pain first began to worry her about four years back. It developed gradually, initially experiencing mainly after prolonged walking or standing. With times, the pain became continuous restricting her day today activities. She took treatment for her knee pain on and off, with the courses of treatment ranging from few days to few months, in few occasions. Despite treatment and intermittent attending to physiotherapy clinic, she got gradual worsening of her knee condition.
She had received intra articular injections in three occasions, (likely intra articular steroids) which gave her temporally relief ranging from few weeks to sometimes few months. Few moths ago she had been told that she might need joint replacement in future if she to obtain accepted mount of mobility.

Although she admitted to a cardiology unit with main complaining of body swelling and shortness of breath, she had a considerable worry about her knee joint problem.

PAST MEDICAL HISTORY
Apart from the above described knee problem, her past medical history was not significant. She did not give a history of hypertension, diabetes mellitus, coronary heart disease or bronchial asthma. She did not have any history of psychiatric illness too.

DRUG HISTORY
She had been taking non-steroidal anti-inflammatory drugs on and off, duration ranging from few days to one to two months in few occasions. In addition, she used to take brufen or voltaran when she experienced severe discomfort during the periods when she was not on any particular drug course.

On three occasions, she had intra articulr injections into her right knee joint. She was not taking any antipsychotic or any other potentially weight gaining drugs. She did not give any history of allergy to drugs or food.

FAMILY HISTORY
She had three sisters and three brothers. Her mother had hypertension and died fallowing a stroke at the age of sixty-five. Father died fallowing a febrile illness. (Probably due to pyelonephritis) One sister is on life long thyroxin for hypothyroidism and her fatty younger sister was under investigation for infertility. No sibling was suffering from hypertension, diabetes mellitus or coronary heart disease.

SOCIAL HISTORY
She was living with her husband in there own house. All her three children ware married and living separately. She was a schoolteacher at near by school and her husband was a pensioner. Their monthly income was over thirty thousands rupees and had substantial amount of money in banks. She was unable to do her day today activities freely due to the associated knee disability and her large body, especially for the last six months.

DIATARIC HISTORY
In addition to three large meals, which were mainly consisted of carbohydrates, she took frequent snacks in between. In spit of having knowing that she was overweight, genuine attempt had not been made about her dieting. History did not suggest binge eating or night eating behavioural patterns.




OBSTETRICS HISTORY
All the three children were bone through normal vaginal delivery without significant complications. There was no history of abortions or stillbirths. She had not undergone any investigations for infertility and did not give a history of difficulty in conception in the past.

MENSTRUAL HISTORY
She had menopause at the age of 46 years and until then her periods had been regular and normal.

EXAMINATION
She was grossly obese. (See fig 5:1)
Following measurements were obtained.

Height : 145 cm
Weight : 79 kg
Waist : 104 cm
Hip circumference : 120 cm
Body Mass Index (BMI) : 37.6 kg/m2
West to hip ratio (WHR) : 0. 866



She was not pale or icteric and there was no xanthalasma or xanthoma. In her face, mild degree of hirsutism noted. Apart from that, there were no other cushinoid features such as plethora, acne, thin skin, easy bruising and skin striae ect. Her thyroid gland was impalpable. There was a milder degree of right ankle swelling and verricourse veins were seen in the same limb. (At the greater saphenious region)

Cardiovascular system examination revealed normal, regular pulse with a rate of 76 beats per minute and blood pressure of 170/ 100 mmHg in both arms. Internal jugular venous pulsation did not see in the neck. Apex beat could not locate due to obesity but trachea felt centrally in the neck. No thrills or para-sternal heave felt.
Fig 5:1
Resent photograph of the patient
Her first and second heart sounds heard softly and there were no murmurs. Third or fourth heart sounds were absent.

Respiratory rate was about fourteen cycles per minute and air entry was equal in both lungs. Few occasional basal crepitations heard at both lung bases but there were no other abnormalities.

No organomegally found in the abdominal examination. Her higher functions were within normal limits and central nervous system examination was unremarkable.
Fundocopy did not show evidence of hypertensive retinopathy or papilloedema and confrontational visual field examination was normal. Her ankle jerk relaxation was normal.

Both knee joints were moderately swollen with moderate effusion but not warm on palpation. Crepitations felt over both knee joints with movement and movements were restricted to a moderate degree due to an associated pain. No obvious deformity or laxity of the ligaments at the joints was noted. Other joints did not show obvious abnormality. She demonstrated a waddling type of gait due to marked obesity and legs looked stiff due to the knee abnormality.

PROBLUMS IDENTIFIED
1. Elevated blood pressure

2. Obesity, which may be primary or secondary.

3. Moderate to severe “osteo arthritis” of both knee joints.

4. Obesity and associated knee joint problem causing significant limitation to her day today activities, which was a major concern to her.


DIFFERENTIAL DIAGNOSIS FOR BODY SWELING
1. HYPOTHYROIDISM WITH PERICARDIAL EFFUSION AND/OR CARDIOMYOPATHY
Although typical symptoms of hypothyroidism was lacking, atypical presentation is comment especially in old age. Soft, almost inaudible heart sounds are compatible with pericardial effusion but on the other hand, it could well be due to the obesity itself. In this setup, elevated jugular venous pressure is not mandatory because shortness of breath on effort may not be due to resting heart failure but due to inability of the heart to meet increased demand on effort. Weigh gain was well compatible with hypothyroidism.

Another reason that justified considering hypothyroidism was that is an easily treatable condition. In the absent of features of hypopituitarism, pituitary disease causing hypothyroidism was unlikely in this patient, instead primary type of hypothyroidism was more likely here.

2. CHRONIC HEART FAILURE
Presence of body swelling, shortness of breath on effort and few basal crepitations in the lungs were compatible with heart failure. As there was no history of coronary artery disease, ischemic heart disease or other common illnesses that predispose to heart failure, and more insidious onset of the symptoms, an uncommon aetiology like amyloidosis or cardiomyopathy should consider here. Hypertension in our patient was not such chronic and severe (No much retinal changers) to cause heart failure.

However absence of tachycardia, third heart sound, elevated jugular venous pressure, and cardiomegaly (clinically) was against this diagnosis. In heart failure, oedema is marked in dependent parts and it is pitting. However, in our patient the body swelling seemed due to excess body fat rather than due to extra cellular fluids. Associated pitting oedema localized to right ankle might well be due to the varicose veins of the leg.

3. CUSHING’S SYNDROME
Although classical features of Cushing’s syndrome were lacking in this patient, presence of marked obesity, hirsutism and hypertension warranted considering this diagnosis. However associated obesity in this patient was not classically trunkal and there was no other more specific features of Cushing’s syndrome, like thin skin, striae ect.
.
4. CHRONIC RENAL FAILURE
This was a very remote possibility. This possibility arose not because she was having classical features of chronic renal failure but because she had been taking non-steroid anti-inflammatory drugs for prolonged period. This was a possible aetiological factor for renal damage and insufficiency. It was of course a remote possibility, as the patient did not complain of symptoms of uraemia, for example anorexia, nausea, pruritus ect, but had generalized body swelling. She also did not give a history of previous renal disease or symptoms of chronic renal failure, like nocturea.



5. PATHOLOGICAL OBESITY
Although this diagnosis explained all of the features, it considered later in the differential diagnosis, as it needed exclusion of other possibilities. Obesity could be due to secondary to various causes (Few of which considered as differential diagnoses above and see discussion for details) or it may be of primary in origin. Shortness of breath is a common association in obese people for many reasons.

History and examination did not give clues for a particular aetiology, but worsening of the osteoarthritis for the last four months causing marked reduction of mobility may have precipitated the obesity in her who seemed to be having genetic predisposing as she had overweight siblings.

Her dietary intake too was in keeping with the associated weight gain in recent months. Hypertension commonly associates with obesity.

INVESTIGATIONS
As the preliminary investigations, we did followings.

Urine full report Proteins- Nil
Sugar - Nil

Blood urea 18mg/dl (15-45 mg/dl)

Serum electrolytes K+/ Na+: 145/4.8 mol/l

Serum creatine 0.8 mg/dl (0.7-1.7 mg/dl)

Above renal profile ruled out the possibility of underling renal impairment in this patient.

Full blood count showed haemoglobin of 14.8 g/dl with normal differential counts and platelets. Such good haemoglobin concentration usually does not occur if she had an underline chronic illness. If anaemia was present, that also would have contributed to the shortness of breath and fatigability.

Electrocardiogram Showed sinus rhythm with heart rate of 76/bpm and normal voltage complexes (no electrical alternant).Cardiac axis was normal and there were no electrical evidence of left ventricular hypertrophy.

Chest radiograph Normal lung field, no cardiomegaly

These findings made associated cardiac failure or pericardial effusion unlikely.


Echocardiography Poor echo window. Good left-ventricular function. Ejection fraction was more than 60 percent. No evidence of pericardial effusion.

At this stage, associated cardiac failure or pericardial effusion was ruled out as the cause for her illness.
Skull radiography showing normal pituitary sella

Fasting blood sugar 95mg /dl

Lipid profile Cholesterol 191mg/dl
Triglyceride 166mg/dl
HDL 40mg/dl
LDL 119mg/dl

Impaired glucose tolerance and dyslipidaemia (Hypertrygleceridaemia with high cholesterol and law HDL) are associated with obesity but our patient was having reasonable lipid profile and her fasting blood glucose level was within the normal limit.

Next, we proceeded to investigate for hypothyroidism and Cushing’s syndrome.

Thyroid Stimulating hormone 0.4mU/L. (0.4 - 4 mU/L)

Triiodothyronin 1.3nmol/L. (1.1 - 2.9 nmol/L)

Both these were with in normal limits. With this biochemical profile, associated thyroid dysfunction was unlikely.

24 hours urinary cortisole 158.24nmol/24 hours (9- 180nmol/24hrs)

Overnight dexamethasone suppression test 121 nmol/L (0 – 300nmol/L)

24 hours urinary cortisole excretion is a sensitive test to detect hypercortism, but we coupled it with overnight dexamethasone test to be in safer side, as we do not wanted to miss such diagnosis at this junction. In the absence of any other features suggesting secondary causes for obesity and the fact that this patient had risk behaviour patterns and family history of “obesity”, primary obesity was the likely diagnosis.

Therefore, we made the diagnosis of pathological primary obesity in a patient who had a familial predisposition, which must have made worse by relatively sedentary life style caused by the severe osteoarthritis of the knee joints and excess caloric intake. In addition, obesity in our patient was associated with hypertension that was an additive health hazard for the patient.

FINAL DIAGNOSES
1. Pathological primary obesity (Precipitated by Familial predisposition, sedentary life style caused by severe osteoarthritis of the knee joints and excess caloric diet)

2. Hypertension

MANAGEMENT
In the management, we planed out following goals
I. Management of obesity to accomplish an acceptable weight (see discussion for details) and maintains the achieved weight. This will reduce the debility and associated increased mortality due to obesity in this patient, and helps to normalize the hypertension. This also enables easy mobility and reduces the stress on the osteoarthritic knee joints, which help to retard the damaging process operating at the joints. This will help to break down the vicious cycle operating between obesity, osteoarthritis of the knee joints and impaired mobility. (Fig 4:2-See discussion for details).

II. Control of high blood pressure; Hypertension as with obesity is an independent risk factor for increase mortality and mobility. (See fig 4: 4)
III. Management of osteoarthritis of the knee joints to provide symptomatic relief, prevent or retard the progression of the disease and increase the function at these joints. This will enables patient to participate in weight reducing activities as well as in her usual day today activities, which at present she cannot do or does with great difficulty. This will reduce her dependency, which was a main concern of the patient, and improves quality of life to a greater extend.

As the patient’s blood pressure was high, oral Nifedipine SR 20 mg twice daily started. After initial assessment with routine biochemistry, chest radiography, electrocardiogram and echocardiogram, we proceeded to perform special investigations to uncover any possibilities of secondary causes for obesity, mainly hypothyroidism and Cushing’s syndrome. Blood withdrew for, free tri-iodo thyroxin and thyroid stimulating hormone. At the same time, arrangements were made for over-night dexamethasone suppression test and 24 hours urinary cortisole estimation.

Out of the above two tests for Cushing’s syndrome, 24 hours urinary cortisole testing is a much superior test for detecting hypercortism.
Ideally, this test should do thrice to make it more sensitive, but in our patient, for practical and personal reasons, we coupled single estimation with overnight dexamethasone suppression test. Of course, if Cushing’s syndrome was strongly suspected, we would have done another two collections of urine, to test for cortisole.

Hypertension was detected for the first time in this admission and it was an additive risk factor associated with obesity. As impaired glucose tolerance and dyslipidaemia can be associated with both of these conditions, blood was taken for lipid profile and fasting blood sugar.
There was moderate degree of swelling at the knee joints and the movements at the joins were restricted to a greater degree. The later was mainly due to the associated pain. We offered paracetamol for the pain. Obesity and osteoarthritis in this patient was closely related and it had operated in a vicious cycle (See fig 4:2). Obesity, which contributed to the development and progression of the osteoarthritis made the patient more inactive, which in turn made the obesity worse.
Fig 4:2
The vicious cycle was operating in our patient, causing obesity and osteoarthritis of the knee joints

Obesity



Decreased mobility stress on the KJ



Osteoarthritis
Calculated waist to hip ratio was 0.866. Risk associated with central fat is significantly high when the waist to hip ratio is more than 0.85. Therefore, our patient was in high-risk group, which warranted active intervention to reduce the risk.

Body mass index of our patient was 37.6kg/m2 and it was in the obesity range. (25 – 30 overweight, > 30 obese). Adjusted body mass index for metabolic variants (see discussion bellow) was 42.6, which was even higher. General agreement is that, if the adjusted body mass index is above 35, treatment with medications in addition to healthy diet and exercise are indicated.

Before discharging, instructions were given to maintain a diary, regarding the type of food, related occasions, time of the day, quality and quantity of the food taken. This will help us to plain out behavioural therapies and gives us a clear idea about her dietary practices. Patient was given adequate encouragement and stimulation to get the maximum compliant.

Exercise alone has relatively little effects on weight reduction, but it certainly helps to prevent the abdominal obesity, maintain the achieved weight and has many more additional advantages (See discussion and Fig 4: 3). As the patient was having disabling knee osteoarthritis, which restricted her doing exercises, instructions were given to perform exercises like leg rising, exercises to the hip and shoulders to avoid excess weight and stress on the diseased knee joints. We taught exercises to strengthen the adjoining mussels of the knee, which will help to support the knee joint against stress. Active and passive movements at the knee joints were encouraged so that it will help to preserve the mobility at the knee joints. Advice gave to wear footwears with well-cushioned sole to facilitate smooth transmission of weight through the legs. Other types of domestic therapies like heat or cool application, acupuncture ect were encouraged, although the effects some people get with these kind of therapy are mainly due to their placebo effect.

Fig 4:3

Dietaric advice was given to reduce the quantity of food, to avoid carbohydrate-containing foods (to moderate degree-Total energy content 30 to 40 %) and not to restrict fats as to provide less than 30% of the total energy. She was asked to avoid refine sugar completely, and to take good quality fats instead of saturated fats. The idea was to provide a diet that contains slightly deficit sum of energy than required for routine daily activities. So that there will be break down of body energy reserves to obtain deficit amount of energy.

Before discharge, we did not start any pharmaceutical agent to control the obesity but planed for subsequent intervention, after observing the response to initial modifications of diet and programmed exercising.

As she required specialist advice for the knee joints osteoarthritis, we directed her to a rheumatology clinic.

Inquiry made after a week, over the phone, to find out the current situation. No change had occurred in her weight. (Neither gain or no loss of weight) She had sought rheumatological opinion. In addition to pain-reliving agents, paracetamol and tremadol, condroprotective agents, Glucosamino-glycants and chondroitine, had given for the osteoarthritis. They also have planed for intra-articular injection of hyaluronic acid derivatives and arthroscopic irrigation of the joints in future. She had told about the important of weight reduction and had warned, if damage continued she would need a major surgical procedure like arthroplasty in future.

DISCUSSION
Obesity is a chronic disorder that confers serious risk for the development of diabetes mellitus, hypertension, dyslipidaemias, heart disease, gall bladder disease, osteoarthritis and certain forms of cancers1. Obesity per say is an independent risk factor for increased mortality, as high cholesterol and high blood pressure. (See fig: 4: 4 below) Prevalence of obesity has increased slowly until 1988.
It has increased by thirty percent during the last decade in the United State. The pattern seems similar in most of the other countries. Obesity has many types and different degree.

Definitions of obesity and overweight
Overweight : Refers to weight above the normal range.

Obesity : Define by the presence of excess fat.

In practice, the difference between obesity and the overweight is made based on the Body Mass Index.

BMI = Body weight in Kg into Stature (Height in squired meters) Kg/m2.
Fig: 4: 4
Obesity is an independent risk factor for death
According to the body mass index, overweight is defined as BMI between 25- 30 and obesity as BMI more than 30 Kg/m2.

Our patient’s body mass index was 37.6 Kg/m2, which was in the obesity range. This simple body mass index, dose not considers the associated metabolic derangements and other risk factors of the patient. So Adjusted Body Mass Index can calculate using the following chart (See fig: 4: 5). Adjusted BMI correlates more closely with the associated morbidity and mortality than the simple BMI.
Our patients adjusted body mass index was 42.6, which was significantly higher than the simple body mass index.
When estimating the cardiovascular and other risk associated with obesity, regional fat distribution must be taken in to account. Pattern of fat distribution has a relation ship to the associated risk. For example, patients with predominantly abdominal obesity are at increased risk of atherosclerosis, hypertension, diabetes mellitus, and gallstones and in females, breast cancer.
Fig4:5


Abdominal fatness can evaluate clinically by measuring waist to hip ratio. (MHR) Although Computered tomography (CT) and Magnetic resonance image (MRI) are more accurate in determining abdominal fatness, they are not usually indicated for this purpose alone.

In our patient, the wrist to hip ratio was 0.866. Women with WHR more than the 0.85 are considered to have a higher morbidity and mortality rates. (See fig: 4: 6). Therefore, our patient was not only obese but also had the worse form of fat distribution too.
(See fig4: 7).
Fig: - 4: 6





Fig: - 4:7

Obesity is a multifactoral disease. It can results from divers aetiological factors. Genetic factors as well as environment factors are directly or indirectly involved in the causation of obesity. (See fig 4: 7) In most cases, these actors contribute to produce the disorder in susceptible patients.

Fig 4:8.

Aetiopathology of obesity
Five genes have identified in animal of which, mutation causes obesity in them and some of them appears too important in humans in the genesis of obesity2. Out of all genes, leptin gene and leptin receptor gene are important in the development of obesity3. Leptin gene code or proteins call leptin4. Leptin binds to specific receptors (Leptin receptors). Leptin receptors are widely distributed in the body. Leptin is produce in the fat cells and in the placenta. It signals the brain about the quantity of stored fat5. Therefore, leptin functions as a negative feedback “adepostatic” signals to the brain centres controlling energy intake6. Leptin deficiency is therefore associated with obesity in humans6.

Obesity is a feature of at lease twenty-four Mundelein disorder7. Majority of these are autosomal dominant, ten are autosomal recessive, and the rest inherit as x link patterns.
The Bardet-Biedle and Prader-Wili syndromes are probably the best-known example of these.

In evaluating patient having obesity, attempts should make to find out possible secondary causes for obesity, as well as to identify associated co-morbid conditions. Presence of high blood pressure and osteoarthritis, for example, in our patient, were important co-morbid conditions that alter the clinical cause of the obesity. Bellow shows the algorithm for evaluating the obese individuals. (Fig 4:8)


Health hazards associated with obesity.
Mortality
There is increased risk of death in-patient with body mass index more than 30 compared to that of less than thirty.
In nurses’ health study, the death rate rose progressively in women with body mass index above 29 kg/m2.
In American cancer society, cancer prevention stud, all with BMI above 29 kg/m2 have shown increase mortality.


Morbidity
In Swedish Obese Subjects Study followed untreated obese subjects with BMI averaging 38 kg/m2, for period of three years. Two years incidents of followings were observed.
Hypertension: 13.6 %.
Diabetes mellitus: 6.3 %.
Hypertrigleceridaemia: 7.7 %.
Hypercholesterolemia: 12.1 %.
Law HDL: 8.6 %.
Hyperinsulinaemia: 6.7 %.



Fig 4: 9
Algorithm for evaluation of the obese individuals


In Swedish obesity study for example, hypertension was present at baseline in approximately one half of the subjects. Weight gain also associated with an increase risk of hypertension8. The relative risk of hypertension in these women who gain weight of 5 to 9.9 kg and, equal or more than 25 kg of body weight was 1.7 and 5.2 respectively.

It is estimated that control of obesity would eliminate forty-eight percent of the hypertension in white population and twenty-five percent in blacks.

Importantly for each one mm decline of diastolic blood pressure, the risk of myocardial infarction decreased to two to three percent9. Persistent obesity not only raises the blood pressure but also make the hypertension more difficult to control10.

Our patient’s body mass index was 37.6 kg/m2 and she was hypertensive too. So here, control of obesity is important because, not only it improves the quality of life but also it makes associated hypertension easier to control. As evidence suggest it is a primary preventive strategy, so that it offers a protection against other morbid conditions associated with obesity.

In addition to above morbidity associations, certain forms of cancers occur more frequently in obese subjects11. For example, obese people have increased risk of cancer of gallbladder and endometrium. In both sexes, obesity has identified as a risk factor for cancer of gastric cardia and gastro-oesophageal junction11.



Obese individuals are often exposed to public disapproval because of there fatness. In study over 10 000 adolescents, women who were over weight completed fewer years of school (0.3 years less), were less likely to marry (20 % less likely), has less house hold income ($ 6.71 less per year) than women who were not obese.

Management of obesity
Obesity is usually, cannot be cured and majority of obese patients required chronic long-term treatment. The rationale for weight loss in obese subjects is that obesity increases health risks.

Framingham study led to the following conclusion. If every one were at optimal weight there would have 25 % less coronary heart disease, 35 % less congestive heart failure and brain infarcts.(5-8”).

Treatment regimes
Although our patient had hypertension and osteoarthritis in association of obesity, she carries an increased risk of developing coronary heart disease, dyslipidaemia and diabetes mellitus, if she continued to gain weight or if she continued to remain obese. Therefore, there will be significant mortality and morbidity benefits if we can reduce and maintains an acceptable weight in this patient.



Treatment options available for obesity are,
Behavioural modifications
Dietetic therapies
Exercise
Drug therapy
Surgical therapy

In general behavioural modification, dietetic therapy and exercises are applicable for every over weight patients. Adjusted body mass index is a very practical guide to use, in setting up goals and treatment strategies for patients. (See fig 4:9/Fig 4:10)

Our patient’s body mass index was 37.6kg/m2. For patients with body mass index above 35kg/m2, interventions with medications are recommended. (See fig4:10) The goal is to reduce weight at lease by fifteen percent or reduction of body mass index more than three BMI unites.

Behavioural modifications
There are only few studies that have done to see the effect of behavioural therapy on the reduction of weight in obese subjects. Satisfactory results have observed in all of the studies12. For example in a one-year study of 590 subjects receiving behavioural therapy, weight loss averaged 5.8 kg, although 17.5 percent were either at or above the base line



Fig: 4:10

weight13. In another study among the 426 subjects followed for two years, the mean weight loss was 6.9 kg in 116 men and 4.2kg in 310 women. The drop out rate were interestedly were low, 10 % to 17 %. Few examples for behavioural therapy are,

· Identifications of the kind of food eating and the settings in which eating occur. Using these records, the subject can identify the situations where eating occur. Behavioural therapy includes avoidance of such situations and times.

· The simplest involve the restriction of the number of places or avoid eating during a certain time interval for example from 8 am to 12 noon.

· Other techniques include picking up glasses of water in between each bite or chewing a food a definite number of times.
The goal is to separate the event that trigger eating from the eating itself.

Another mode of behavioural therapy includes manipulating the consequence of eating for self-rewards. Subject should learn to say no and develop positive self-talk.

Our patient was asked to maintain a diary on type of foods eating and places of eating these will enable us to plane out behavioural modifications more rationally.

Dietary therapies
The rate of weight loss is directly related to the difference between the patient’s energy intake and energy expenditure. An average deficit of 500 kcal/day, should results in weight loss of 0.45 kg/week. However, there is wide variability, because energy requirements are influence by sex, age and genetic factors. Men tend to loos more weight than females of similar height and weight.

Metabolic rate declines by approximately two percent per decade. Because of this reason, alder the patient has lower metabolic expenditure and therefore loose weight more slowly. Conventional diets are defined as those bellow energy requirement but above 800 kcal per day.

The carbohydrate content of the diet is and important determinant of short term weight loss. However, this largely represents fluid rather than fat loss. Protein brake down is an expected part of weight loss. High dietary nitrogen content is required to minimize nitrogen loss when caloric content is bellow that required maintaining body weight14. The usual recommendation is 0.8 g/kg of protein per day. Almost all dietary guidelines recommend a reduction of daily intake of fat to thirty percent of energy intake or less (Diet and health report). Patient adhering to very law caloric diet have reduction in blood pressure. Care must be taken as hypotension can occur when treating with anti-hypertensive.

Frequency of meals
Person who eats less than two meals per day have greater skin fold thickness than do who eat more than two meals per day14. Eating one or two meals, a day is also associated with an increase in serum cholesterol, as compared with eating six or more meals per day. It would therefore seem desirable to eat five meals per day at whatever level of protein is selected.

One explanation for the effect of the frequency of food intake may relate to the quantitative secretion of insulin. Each release of insulin will be smaller and the lipogenic effects are less with frequent meals. In addition, the stimulation for storage of large meals has to be greater, and the subsequent release of nutrients may be slower. We gave clear instruction to the patient, to eat less quantity of meals (within instructed amounts and quality) four to five times a day rather than taking two large meals, omitting the dinner.



Drug therapy
Drug therapy may be a helpful component in the treatment of overweight subjects, along with diet, exercise, and behaviour modification. However, the role of drug therapy has been questioned, because of concerns about efficacy, the potential for abuse, and side effects.

The decision to initiate drug therapy in overweight subjects should be made only after a careful evaluation of risks and benefits. Adjusted body mass index is a reasonable guide for this. (See fig 4:5) Adjusted body mass index take in to the consideration of co morbid conditions such as diabetes mellitus, dyslipidemia, hypertension, and heart disease.

Goals of any therapy
The ideal outcome of a return to normal body weight is unrealistic. Weight loss should exceed 2 kg during the first month of drug therapy, fall more than 5 percent below baseline by three to six months, and remain at this level to be considered effective.

In drug trials, weight loss of 10 to 15 percent is considered a good response and loss exceeding 15 percent is considered an excellent response. This degree of weight loss should have substantial benefits, including lowering blood pressure and serum lipid concentrations, increasing insulin sensitivity, and reducing hyperglycaemia.


Summery of drugs that can be used in obesity

1. Drugs that alter the fat metabolism
Orlistat- (Xenical®-available in Sri Lanka) is currently the only drug that alters fat metabolism. It does so by inhibiting pancreatic lipases15. This is associated with increased faecal fat excretion. The United States Food and Drug Administration has now approved orlistat for obese patients with an initial body mass index of at least 30 kg/m2 or at least 27 kg/m2 in the presence of other risk factors.

2. Drugs that reduce food intake
Leptin- Obese humans appear to have leptin resistance, because they have high serum leptin concentrations. Human recombinant leptin administration causes decrease in body weight. The decrease in weight is due mostly to loss of fat, but was variable among different subjects. The main adverse effect is local reactions at the injection site. Many develop serum anti-leptin antibodies.

3. Other drugs
a) Sibutramin
b) Phenylpropanolamine (Short term only)
c) Cholesistakini
These drugs are not routinely indicated and their safety and efficacy are not well established.

Surgical therapy
Surgery is another option for patients at high risk of complications of obesity. It has the advantage of being a long-term solution to a chronic physiologic problem.

Few examples are as follows.
Gastric restriction procedures (gastric banding, vertical-banded gastroplasty, and vertical-ring gastroplasty)
Gastric bypass
Biliopancreatic bypass





References
1. Human obesity, JAMA 1995

2. Human obesity, Geen M P 1998 update

3. Clinical Medicine 2000- Leptin and obesity

4. Cloning of obesity genes- R Muffy, et, al, 1994

5. The Leptin pathway; Campfied 1996

6. Leptin and clinical medicine; 1997

7. Genetics of human obesity; Research directions; FASEB J 1997; 11:937

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Case report from King's Mill Hospital - UK

Ciprofloxacine induce tendinitis

Introduction
Tendinopathy after fluoroquinolone is a well recognized but an uncommon adverse effect. Fluoroquinolone is commonly used antibiotic in diabetic patient because of its broad antibacterial activity, relative safety in renal impairment, and good soft tissue penetration. We report a patient with diabetic foot ulcer who has been prescribed ciprofloxacin for a period of 6 weeks.

Case report
Our patient is 62-year-old male with type 2 diabetes for – years. He has been following up in the diabetes fool clinic for a right sided diabetic foot ulcer.
Ciprofloxacin was started on him 6-weeks ago. His uric acid was normal and the rheumatological screen was negative. His serum creatinin was ---. On the fourth week of treatment the patient developed tendinitis involving semimembranosus tendon at the right knee joint and subsequently flexor tendon at the elbow (triceps epicondyle). He was not on any other drug that is known to cause tendinitis. ((His symptoms improved with the discontinuation of the antibiotic)). We concluded that this tendinitis is most likely related to the ciprofloxacin.

Discussion
Tendinitis is a rare adverse reaction described after drugs use. Fluoroquinolones especially pefloxacine, were the most incriminated (2). Fluoroquinolones are relatively safe, effective broad spectrum antibiotics. As their use becomes more frequent, so will the adverse side effects. Risk factors for the development of fluoroquinolone-induced tendinopathy are age, renal failure, corticosteroid use, diabetes mellitus, hyperparathyroidism, rheumatic disease, gout, participation in sports, and previous tendinopathy from fluoroquinolones (1, 5, 6, 7, 8, 9, 10).
The incidence of fluoroquinolone-induced tendon injury in an otherwise healthy population is not well established, but reports suggest that it is low, ranging from 0.14% to 0.4% (11, 12, 13). The incident of tendinitis is slightly more common in male (1.9 to 1-male female ratio) and the age over 60 years is associated with high risk. (5, 6, 7, 8, 10).
The median duration of fluoroquinolone treatment before the onset of tendon injury can be as early as 2 hours after the first dose and as late as 6 months after treatment was stopped (3).